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8 November 2026

13 Pages

Clinical Characteristics, Management, and Outcomes of Pediatric Noncirrhotic Portal Hypertension: A 25-Year Single-Center Cohort

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Department of Pediatric Gastroenterology, Hepatology and Nutrition, Manisa City Hospital, 45040 Manisa, Türkiye
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Department of Pediatric Gastroenterology, Hepatology and Nutrition, Uşak Training and Research Hospital, 64200 Usak, Türkiye
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Department of Pediatric Gastroenterology, Hepatology and Nutrition, Ege University School of Medicine, 35100 Izmir, Türkiye
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Department of Pediatrics, Ege University School of Medicine, 35100 Izmir, Türkiye
Children2026, 13(11), 1542;https://doi.org/10.3390/children13111542
This article belongs to the Section Pediatric Gastroenterology and Nutrition
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Highlights

What are the main findings?
  • Pediatric noncirrhotic portal hypertension was associated with substantial variceal bleeding and hypersplenism despite generally preserved hepatic synthetic function.
  • Following shunt surgery, weight and height standard deviation scores and several hematologic parameters improved significantly at one year, while bilirubin levels increased.
What are the implications of the main findings?
  • Clinical follow-up should address growth and hematologic abnormalities alongside the prevention and management of gastrointestinal bleeding.
  • The substantial burden of portal hypertensive complications highlights the need for individualized, multidisciplinary treatment strategies in children with NCPH.

Abstract

Background/Objectives: To describe the clinical characteristics and outcomes of pediatric noncirrhotic portal hypertension (NCPH), focusing on postoperative growth, hematologic, and biochemical changes. Methods: This retrospective study included children diagnosed with NCPH between 2000 and 2024. Clinical characteristics and treatments were reviewed. Paired preoperative and one-year postoperative measurements were compared using the Wilcoxon signed-rank test. Results: Ninety-four children were included (median diagnostic age, 4 years). Prehepatic disease accounted for 75.5%, predominantly portal vein thrombosis (69.1%). Splenomegaly and thrombocytopenia occurred in 88.3% and 62.8%, respectively. Varices were identified in 76/90 patients (84.4%), and 60/87 (69.0%) experienced gastrointestinal bleeding. Shunt surgery was performed in 53 patients (56.4%), primarily for variceal bleeding (47/53); postoperative bleeding occurred in 3/53 (5.7%). Among 37 patients with paired anthropometric data, median weight SDS increased from −0.56 to 0.00 (p = 0.001) and height SDS from −0.63 to 0.40 (p = 0.002), without a significant change in BMI SDS. Among 48 patients with paired laboratory data, hemoglobin increased from 10.15 to 12.00 g/dL (p < 0.001) and platelets from 83.3 to 112.7 × 103/µL (p = 0.009); white blood cell counts remained unchanged. Total bilirubin increased from 0.71 to 0.91 mg/dL (p = 0.003), without significant changes in albumin or INR. Bilirubin changes did not differ significantly between distal splenorenal shunt and Meso-Rex bypass. Conclusions: Shunt surgery was associated with postoperative bleeding in 5.7% of patients and significant improvements in weight, height, hemoglobin, and platelet counts at one year. Bilirubin increased without evidence of deteriorating hepatic synthetic function; its clinical significance remains uncertain.

1. Introduction

Portal hypertension in children differs from that in adults in both its underlying etiologies and clinical course. While cirrhosis and progressive hepatic dysfunction predominate in adults, pediatric portal hypertension often occurs with preserved hepatic function [1,2]. Consequently, long-term morbidity in affected children is largely driven by complications of portal hypertension rather than hepatic insufficiency. These include variceal bleeding, hypersplenism and associated cytopenias, impaired somatic growth, and reduced quality of life, underscoring the need for sustained surveillance and management throughout childhood [1,2].
Noncirrhotic portal hypertension (NCPH) encompasses a heterogeneous spectrum of prehepatic, intrahepatic, and posthepatic disorders. In children, extrahepatic portal vein obstruction (EHPVO) is the most common prehepatic cause, whereas congenital hepatic fibrosis, porto-sinusoidal vascular disease, nodular regenerative hyperplasia, and other vascular disorders are less common etiologies [3,4,5]. Despite generally preserved hepatic synthetic function, children with NCPH may experience substantial morbidity from recurrent variceal bleeding, hypersplenism-related cytopenias, and impaired growth [6,7]. Because these patients often have a prolonged disease course with preservation of the native liver, they may require repeated endoscopic, radiological, or surgical interventions and continued multidisciplinary care throughout childhood and into adulthood [8].
Advances in pediatric endoscopy, surgical shunting, and interventional radiology have expanded the therapeutic options for children with portal hypertension. However, evidence regarding the long-term course and outcomes of pediatric NCPH remains limited. In particular, longitudinal data integrating bleeding control, somatic growth, and hematologic recovery are scarce. Such information is important for defining the long-term burden of NCPH and guiding management and follow-up throughout childhood [9,10,11].
Using data from a 25-year experience at a tertiary pediatric referral center, this study aimed to characterize the etiological spectrum, clinical features, management, and outcomes of children with NCPH.

2. Materials and Methods

2.1. Study Design and Population

We conducted this retrospective, single-center cohort study at the Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Ege University Faculty of Medicine Hospital, a tertiary referral center. Medical records of pediatric patients (<18 years) diagnosed with noncirrhotic portal hypertension (NCPH) between January 2000 and December 2024 were retrospectively reviewed. Patients with prehepatic, intrahepatic, or posthepatic causes of NCPH were included. Patients with cirrhotic portal hypertension or insufficient clinical data for evaluation were excluded. A minimum follow-up duration of 1 year was required for inclusion.

2.2. Diagnosis and Classification

The diagnosis of NCPH was based on clinical, laboratory, radiological, endoscopic, and, when available, histopathological findings, with exclusion of cirrhosis. Etiologies were classified according to the anatomical level of portal venous obstruction as prehepatic, intrahepatic, or posthepatic based on clinical findings, laboratory investigations, and imaging studies. Prehepatic causes included extrahepatic portal vein obstruction (EHPVO), encompassing portal vein thrombosis and splenic vein thrombosis. Intrahepatic causes included congenital hepatic fibrosis, idiopathic noncirrhotic portal hypertension/nodular regenerative hyperplasia, and porto-sinusoidal vascular disease (PSVD). Posthepatic causes included Budd–Chiari syndrome and sinusoidal obstructive syndrome. Cirrhosis was excluded through a comprehensive evaluation of clinical, biochemical, and radiological findings. Liver biopsy was performed in selected patients when additional histopathological evaluation was considered necessary.

2.3. Data Collection

Demographic data, including age at diagnosis and sex, anatomical classification and underlying etiology of portal hypertension, presenting clinical features, anthropometric measurements, laboratory parameters, radiological and endoscopic findings, treatment modalities, and follow-up outcomes were collected from medical records. Anthropometric measurements included weight, height, and body mass index (BMI), which were expressed as age- and sex-specific standard deviation scores (SDS).
Laboratory parameters included hemoglobin, hematocrit, white blood cell and platelet counts, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), total and direct bilirubin, albumin, and international normalized ratio (INR). Thrombophilia investigations and identified thrombophilic abnormalities were recorded when available.
Radiological data included liver and spleen sizes and portal and splenic vein measurements. Endoscopic findings included the presence, location, and grade of gastroesophageal varices, along with details of endoscopic interventions. Gastrointestinal bleeding episodes before and during follow-up were also recorded.
For patients undergoing portosystemic shunt surgery, anthropometric and laboratory parameters were recorded immediately before surgery and at the 1-year postoperative follow-up to evaluate changes after surgical intervention.

2.4. Statistical Analysis

Statistical analyses were performed using IBM SPSS Statistics version 29.0 (IBM Corp., Armonk, NY, USA). Continuous variables were assessed for normality using the Shapiro–Wilk test and visual inspection of distribution plots. Normally distributed variables were expressed as mean ± standard deviation, whereas non-normally distributed variables were presented as median and interquartile range (IQR). Categorical variables were summarized as frequencies and percentages. For patients undergoing portosystemic shunt surgery, paired anthropometric and laboratory measurements obtained before surgery and at the 1-year postoperative follow-up were compared using the Wilcoxon signed-rank test. All tests were two-sided, and a p value < 0.05 was considered statistically significant.
In addition to analyzing continuous hematologic parameters, changes in anemia, thrombocytopenia, and leukopenia were evaluated using paired preoperative and one-year postoperative measurements. Anemia was defined according to age- and sex-specific hemoglobin thresholds recommended by the World Health Organization (2024) [12]. Thrombocytopenia was defined as a platelet count below 150 × 103/µL. Leukopenia was defined as a white blood cell count below the age- and sex-specific 2.5th percentile of the pediatric reference intervals reported by Özgen et al. [13]. One patient whose estimated age at surgery exceeded the upper age limit of these reference intervals was excluded from the categorical leukopenia analysis. The proportions of patients with normalization of pre-existing cytopenias were calculated, and changes in paired categorical outcomes were assessed using the two-sided exact McNemar test.

3. Results

A total of 94 children with noncirrhotic portal hypertension were included in the study. Of these, 51 (54.3%) were male and 43 (45.7%) were female. The median age at diagnosis was 4.0 years (interquartile range [IQR], 2.0–10.0; range, 0–17 years). Gastrointestinal bleeding was the most common presenting manifestation, occurring in 40 patients (42.6%), followed by abdominal pain in 17 (18.1%) and abdominal distension in 16 (17.0%). Seven patients (7.4%) were referred from another center. Presenting manifestations are summarized in Table 1. Splenomegaly was the most common physical finding, observed in 83 patients (88.3%), whereas hepatomegaly and ascites were present in 24 (25.5%) and 21 (22.3%), respectively.
Table 1. Presentation at diagnosis.
At diagnosis, the median hemoglobin concentration was 10.6 g/dL (IQR, 9.02–11.80), white blood cell count was 448/µL (IQR, 3267.5–6562.5), and platelet count was 103 × 103/µL (IQR, 68.25–172.25). Thrombocytopenia, defined as a platelet count <150 × 103/µL, was present in 59 patients (62.8%). Liver biochemical and synthetic parameters were generally preserved, with median ALT of 19 U/L (IQR, 15–30), AST of 35 U/L (IQR, 27–41), albumin of 4.10 g/dL (IQR, 3.68–4.51), and INR of 1.20 (IQR, 1.08–1.30). Baseline laboratory findings are shown in Table 2.
Table 2. Baseline laboratory findings.
Prehepatic disorders were the predominant etiological category, accounting for 71 of 94 patients (75.5%), whereas 23 patients (24.5%) had intrahepatic causes of NCPH. No posthepatic causes were identified. Table 3 presents the etiological distribution.
Table 3. Etiological distribution of noncirrhotic portal hypertension.
Radiological measurements of the portal and splenic veins were available for 63 and 67 patients, respectively. Liver biopsy was performed in 4 of 94 patients (4.3%). Histopathological examination revealed congenital hepatic fibrosis in two patients and findings consistent with idiopathic noncirrhotic portal hypertension in the other two. Upper gastrointestinal endoscopy was performed in 90 of 94 patients (95.7%), and varices were identified in 76 of those examined (84.4%). Detailed radiological and endoscopic findings are presented in Table 4.
Table 4. Radiological and endoscopic findings.
Data on the number of gastrointestinal bleeding episodes were available for 87 patients. Of these, 60 (69.0%) had at least 1 documented episode. Eighteen patients (20.7%) had 1 episode, 15 (17.2%) had 2 episodes, and 27 (31.0%) had 3 or more episodes. Additionally, 27 (31.0%) had no documented episodes. Among patients who subsequently underwent portosystemic shunt surgery, variceal bleeding was the indication for surgery in 47 of 53 patients (88.7%).
Treatment strategies varied according to clinical presentation and disease course. Beta-blocker therapy was administered to 73 patients (77.7%), including 20 (27.4%) who received treatment exclusively for primary prophylaxis, 38 (52.1%) exclusively for secondary prophylaxis, and 15 (20.5%) who received both primary and secondary prophylaxis at different stages of their clinical course. Additionally, 31 patients (33.0%) underwent at least one endoscopic therapeutic intervention. Portosystemic shunt surgery was performed in 53 patients (56.4%), 16 of whom also received endoscopic treatment (Table 5).
Table 5. Treatment modalities and indications for portosystemic shunt surgery in children with noncirrhotic portal hypertension.
Among 53 patients who underwent portosystemic shunt surgery, postoperative gastrointestinal bleeding was documented in 3 (5.7%). Mortality or infections requiring hospitalization were not documented in 94 patients during follow-up. Paired anthropometric measurements before surgery and at 1 year after shunt surgery were available for 37 patients. Median weight SDS increased from −0.56 (IQR, −1.50 to 0.31) before surgery to 0.00 (IQR, −1.35 to 1.03) at 1 year (p = 0.001). Median height SDS increased from −0.63 (IQR, −1.78 to 0.92) to 0.40 (IQR, −0.59 to 1.17) (p = 0.002). BMI SDS did not change significantly (p = 0.255).
Paired laboratory measurements were available for 48 patients for most parameters. At 1 year after shunt surgery, the median hemoglobin increased from 10.15 to 12.00 g/dL (p < 0.001), hematocrit from 31.30% to 36.70% (p < 0.001), and platelet count from 83.3 to 112.7 × 103/µL (p = 0.009). MCV also increased significantly (p < 0.001), whereas white blood cell count did not change significantly (p = 0.743). The median AST decreased from 34.5 to 26.0 U/L (p = 0.020), whereas ALT, GGT, and ALP remained unchanged. Total and direct bilirubin increased significantly at 1 year (p = 0.003 and p = 0.002, respectively), while albumin and INR showed no significant changes. Changes in anthropometric and laboratory parameters following shunt surgery are presented in Table 6.
Table 6. Changes in anthropometric and laboratory parameters from baseline to 1 year after portosystemic shunt surgery.
To further evaluate the hematologic manifestations of hypersplenism, an additional analysis was conducted in 48 patients with paired preoperative and one-year postoperative measurements. Preoperative anemia was identified in 39 patients, of whom 20 (51.3%) achieved normalization of hemoglobin levels at one year. Thrombocytopenia was present in 37 patients before surgery and resolved in 7 (18.9%), whereas it persisted in 30 (81.1%). Preoperative leukopenia was identified in 30 of 47 evaluable patients (63.8%), of whom 8 (26.7%) achieved normalization at one year, whereas leukopenia persisted in 22 (73.3%). Six patients developed leukopenia postoperatively. Changes in anemia status were statistically significant (p < 0.001), whereas changes in thrombocytopenia and leukopenia status were not significant (p = 0.180 and p = 0.791, respectively). Postoperative spleen size measurements were unavailable, precluding assessment of changes in splenomegaly.
When bilirubin changes were analyzed by shunt type, the median total bilirubin increased from 0.69 mg/dL (IQR, 0.46–0.93) to 1.05 mg/dL (IQR, 0.77–1.52) 1 year after distal splenorenal shunt surgery (p = 0.004). In contrast, no significant change was observed after Meso-Rex bypass (0.76 [IQR, 0.58–0.97] vs. 0.89 [IQR, 0.70–1.10] mg/dL; p = 0.123). Direct bilirubin increased significantly within both groups (p = 0.006 and p = 0.027, respectively). However, the magnitude of change in total and direct bilirubin did not differ significantly between the two shunt types (p = 0.467 and p = 0.672, respectively).

4. Discussion

In this 25-year single-center cohort of children with NCPH, prehepatic disorders predominated, and portal vein thrombosis accounted for most cases. The clinical burden was primarily related to portal hypertension rather than hepatic dysfunction, as reflected by the high prevalence of splenomegaly, thrombocytopenia, gastroesophageal varices, and gastrointestinal bleeding despite generally preserved hepatic synthetic function. More than half of the cohort ultimately underwent portosystemic shunt surgery, primarily for variceal bleeding. In addition to bleeding control, significant improvements in weight and height SDS and in several hematologic parameters were observed at 1 year, whereas albumin and INR remained stable. These findings highlight the substantial morbidity associated with pediatric NCPH and suggest that the benefits of shunt surgery may extend beyond preventing recurrent bleeding to improving growth and hematologic parameters associated with portal hypertension.
Prehepatic disorders were the predominant etiological category in our cohort (75.5%), with portal vein thrombosis accounting for 69.1% of cases. This predominance aligns with previous pediatric studies identifying extrahepatic portal vein obstruction or portal vein thrombosis as a major cause of NCPH in childhood [5,14]. Wojcik et al. reported portal vein thrombosis in 84.6% of 26 children with NCPH, with a mean age at diagnosis of 5.2 years, comparable to the median diagnostic age of 4 years in our cohort [15]. In contrast, a recent pediatric NCPH cohort by Jarasvaraparn et al. showed a more heterogeneous etiological distribution, with extrahepatic portal venous obstruction accounting for 42.8% of cases, followed by congenital hepatic fibrosis (27.0%), nodular regenerative hyperplasia (15.9%), and idiopathic NCPH (9.5%) [16]. The greater predominance of prehepatic disease in our cohort may reflect geographic and etiological differences and the extended 25-year study period.
The clinical phenotype in our cohort was dominated by manifestations of portal hypertension. Gastrointestinal bleeding was the most common presenting manifestation (42.6%), and 69.0% of patients with available bleeding data had experienced at least one documented episode. Splenomegaly was the most prevalent physical finding (88.3%), while thrombocytopenia was present in 62.8% of patients. These findings are broadly consistent with the pediatric NCPH cohort reported by Jarasvaraparn et al., in which splenomegaly and thrombocytopenia were observed in 68.3% and 63.5% of patients, respectively, although gastrointestinal bleeding at presentation was less frequent (31.7%) [16]. Despite the substantial clinical burden of portal hypertension, liver biochemical parameters were generally unremarkable, and hepatic synthetic function was relatively preserved, as reflected by albumin and INR values. This clinical pattern is consistent with previous descriptions of pediatric NCPH [14,17].
Upper gastrointestinal endoscopy revealed varices in 84.4% of examined patients. Esophageal varices were the predominant pattern, occurring either in isolation or in combination with gastric and, less frequently, duodenal varices. This prevalence is comparable to the 86% reported by Jarasvaraparn et al. in children with NCPH [16], although higher rates have been described in cohorts focusing specifically on EHPVO. Gökçay et al. reported esophageal varices in 94.8% of 82 Turkish children with EHPVO [18], while El-Karaksy et al. identified esophageal and fundal varices in 94% and 23%, respectively, of 169 Egyptian children [19]. Beyond their high prevalence, varices may recur or change in distribution following endoscopic treatment. Recurrence of esophageal varices after eradication has been documented in children, and changes in gastric variceal distribution may occur during follow-up [20,21]. These findings highlight the importance of continued endoscopic assessment in children with portal hypertension.
The diversity of therapeutic strategies in our cohort further reflects the complexity of managing pediatric NCPH. This heterogeneity is consistent with the lack of a uniformly accepted management strategy for portal hypertension in children. Shneider et al. emphasized the paucity of pediatric evidence to base management recommendations on [10], while a recent survey by the ESPGHAN Portal Hypertension Special Interest Group demonstrated substantial inter-center variability in screening, primary and secondary prophylaxis, pharmacological therapy, and surgical management [11]. Notably, 16 patients in our cohort received both endoscopic therapy and shunt surgery, illustrating the frequent need for multimodal management in children with clinically significant portal hypertension.
The substantial burden of portal hypertensive complications was reflected in the high rate of portosystemic shunt surgery (56.4%), primarily performed for variceal bleeding (88.7%). Jarasvaraparn et al. reported surgical shunting in 11.1% and TIPS in 3.2% of children with NCPH [16], whereas Di Giorgio et al., in a multicenter cohort of children with noncirrhotic portal vein thrombosis, reported that approximately one-third ultimately required surgical shunting or TIPS during long-term follow-up [22]. The comparatively high rate of shunt surgery in our cohort may reflect the predominance of prehepatic disease and the substantial cumulative burden of variceal bleeding. Despite this high surgical requirement, bleeding control after shunt surgery was favorable, with postoperative gastrointestinal bleeding documented in only 3 of 53 patients (5.7%). This rate closely parallels the pooled postoperative gastrointestinal bleeding rate of 5.6% reported for portosystemic shunts in the systematic review by Yamoto et al. [23]. Similarly, Wojcik et al. demonstrated a significant reduction in hospital admissions for gastrointestinal bleeding following shunt surgery in children with NCPH [15]. Collectively, these findings suggest favorable postoperative bleeding outcomes in appropriately selected children undergoing shunt surgery.
Beyond bleeding control, significant improvements in somatic growth were observed one year after portosystemic shunt surgery. These findings align with previous pediatric studies reporting improved growth after surgical restoration or diversion of portal blood flow. Lautz et al. demonstrated improvement in growth impairment after meso-Rex bypass in children with extrahepatic portal vein obstruction [9], and other pediatric surgical series have reported favorable changes in growth parameters after shunt procedures [24]. The observed improvements in our cohort suggest that the potential benefits of surgical management may extend beyond bleeding prevention to include somatic growth. One year after shunt surgery, hemoglobin, hematocrit, MCV, and platelet counts increased significantly, whereas white blood cell counts remained unchanged. These findings are consistent with those of Wojcik et al., who reported increased platelet counts but stable white blood cell counts after surgical intervention in children with NCPH [15]. The improvements in hemoglobin and hematocrit may reflect a reduced bleeding burden, while the increase in platelet count may be related to alleviation of hypersplenism following portal decompression. Although significant improvements in hemoglobin and platelet counts were observed after shunt surgery, normalization of cytopenias was variable. These findings suggest that hematologic improvement does not necessarily indicate complete resolution of hypersplenism. Nevertheless, these findings should be interpreted with caution. Concurrent medical treatment, nutritional factors, and other clinical variables may have contributed to the postoperative changes. Therefore, these results demonstrate favorable within-patient changes during the first postoperative year rather than establishing a causal effect of the surgical intervention.
Among biochemical parameters, AST decreased modestly after surgery, while ALT, GGT, ALP, albumin, and INR remained stable, reinforcing that hepatocellular and synthetic function was preserved throughout the study period regardless of intervention. A more nuanced finding concerned the post-shunt rise in bilirubin. Total bilirubin increased significantly after distal splenorenal shunt but not after meso-Rex bypass, while direct bilirubin increased significantly within both subgroups. However, when the magnitude of change was compared directly between the two shunt types, neither the total nor the direct bilirubin increase differed significantly between groups, likely reflecting the limited size of the meso-Rex subgroup (n = 13) rather than a true absence of effect. These findings should therefore be interpreted with caution: while the pattern is compatible with the hypothesis that non-restorative, purely decompressive shunting may be less effective than physiologic hepatopedal reconstruction at preventing progression of portal cavernoma cholangiopathy—a recognized long-term biliary complication of extrahepatic portal vein obstruction characterized by biliary strictures, cholestasis, and, in a subset of patients, biochemical or clinical jaundice [25,26]—the present data do not establish a statistically robust difference between shunt types, and this dissociation warrants confirmation in larger, adequately powered cohorts before it can inform shunt-selection practice. This is consistent with prior comparative series suggesting that meso-Rex bypass, by restoring direct hepatopedal flow, may offer advantages over decompressive shunts beyond bleeding control alone [27]. Regardless of shunt type, the consistent rise in direct bilirubin after surgery underscores the importance of routine post-shunt biliary surveillance in children with long-standing EHPVO.

Limitations

This study has several limitations. Its retrospective, single-center design may have introduced selection bias and variability in diagnostic and therapeutic practices. Heterogeneous etiologies and surgical procedures, along with the relatively small Meso-Rex subgroup, limited the interpretation of comparisons between shunt types. Incomplete follow-up data further reduced the sample sizes available for paired analyses, particularly for anthropometric outcomes. Furthermore, standardized postoperative anthropometric and laboratory data were available only at the one-year follow-up, precluding assessment of the long-term durability of the observed improvements. Although the study covered a 25-year period, this reflects the duration of patient enrollment rather than a uniform long-term postoperative follow-up period. Additionally, individual follow-up durations could not be calculated because the required dates were not consistently available in the retrospective dataset.

5. Conclusions

In this 25-year pediatric NCPH cohort, portal vein thrombosis was the predominant etiology, and substantial morbidity occurred despite relatively preserved hepatic function. Portosystemic shunt surgery was associated with a low rate of postoperative gastrointestinal bleeding and significant improvements in growth and hematologic parameters at one year. Although bilirubin levels increased after surgery, the clinical significance of this finding and its relationship to shunt type remain uncertain. These findings highlight the importance of individualized management and comprehensive follow-up addressing not only bleeding control but also growth, hematologic abnormalities, and hepatic biochemical changes. Larger prospective studies are needed to clarify the comparative outcomes of different shunt procedures and the durability of their benefits.

Author Contributions

Conceptualization, B.K. and M.K.; methodology, B.K., D.B. and M.K.; formal analysis, B.K.; investigation, B.K., E.O., E.T.Ç., İ.S.Z. and E.K.T.; resources, Ü.Ç., O.E. and F.Ç.; data curation, B.K. and D.B.; writing—original draft preparation, B.K.; writing—review and editing, D.B., M.K. and F.Ç.; supervision, M.K.; project administration, M.K. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

The study was conducted in accordance with the Declaration of Helsinki and approved by the Institutional Review Board (Ethics Committee) of Ege University Faculty of Medicine (protocol code 26-9T/56, approval date 3 September 2026).

Data Availability Statement

The data presented in this study are available on request from the corresponding author due to institutional ethical and privacy restrictions.

Acknowledgments

The authors thank the medical records staff of the Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Ege University Faculty of Medicine, for their assistance with data retrieval.

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

The following abbreviations are used in this manuscript:
NCPH: noncirrhotic portal hypertension; EHPVO: extrahepatic portal vein obstruction; PSVD: porto-sinusoidal vascular disease; SDS: standard deviation score; BMI: body mass index; IQR: interquartile range; AST: aspartate aminotransferase; ALT: alanine aminotransferase; ALP: alkaline phosphatase; GGT: gamma-glutamyl transferase; INR: international normalized ratio; MCV: mean corpuscular volume; TIPS: transjugular intrahepatic portosystemic shunt; ESPGHAN: European Society for Paediatric Gastroenterology, Hepatology and Nutrition.

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